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Initial Stages of Posterior Vitreous Detachment in Healthy Eyes of Older Persons Evaluated by Optical Coherence Tomography
Eisuke Uchino, MD;
Akinori Uemura, MD;
Norio Ohba, MD, PhD
Arch Ophthalmol. 2001;119:1475-1479.
ABSTRACT
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Objective To promote understanding of the development of posterior vitreous detachment
(PVD) in healthy eyes using optical coherence tomography (OCT).
Methods We studied 209 eyes of 209 healthy volunteers (165 men and 44 women;
mean age, 52.3 years [range, 31-74 years]). In addition to biomicroscopy and
ophthalmoscopy, OCT was performed to obtain high-resolution cross-sectional
images of the vitreoretinal interface in the posterior fundus.
Results The condition of the posterior vitreoretinal interface was classified
as 1 of 5 stages, according to biomicroscopic findings and OCT images relative
to discrete linear signals indicating a detached posterior vitreous face:
stage 0, no PVD (61 eyes [29.2%]); stage 1, incomplete perifoveal PVD in up
to 3 quadrants (100 eyes [47.8%]); stage 2, incomplete perifoveal PVD in all
quadrants, with residual attachment to the fovea and optic disc (26 eyes [12.4%]);
stage 3, incomplete PVD over the posterior pole, with residual attachment
to the optic disc (4 eyes [1.9%]); or stage 4, complete PVD identified with
biomicroscopy, but not with OCT because of instrument limitations (18 eyes
[8.6%]). Stage 1, 2, and 3 incomplete PVD without subjective symptoms was
not recognizable on contact lens biomicroscopy. There was a significant age-related
progression in the condition of the vitreoretinal interface from stage 0 to
stage 4. The superior quadrant was usually the initial site of incomplete
PVD.
Conclusions Optical coherence tomography demonstrates that healthy human eyes have
incomplete or partial PVD beginning as early as the fourth decade of life.
Age-related PVD occurs initially as a focal detachment in the perifovea of
1 quadrant, with persistent attachment to the fovea and optic nerve head,
with a predilection for the superior quadrant. It extends its range slowly
for years and eventually results in complete PVD, associated with release
of vitreopapillary adhesion.
INTRODUCTION
POSTERIOR vitreous detachment (PVD) is one of the most striking age-related
changes in the human eye. According to autopsy studies,1-2
PVD is present in fewer than 10% of persons younger than 50 years, but has
been found in at least one eye in 27% of individuals aged 60 to 69 and in
63% of subjects aged 70 and older. Clinical studies3-8
also reveal a low incidence of PVD in individuals younger than 50. Posterior
vitreous detachment is believed to develop after liquefied vitreous passes
abruptly into the subhyaloid space and separates the posterior hyaloid from
the retina.9-10 However, the actual
process in older persons with healthy eyes remains unknown, because of the
difficulty in identifying its initial stage.11
Optical coherence tomography (OCT) provides high-resolution cross-sectional
images of the posterior vitreous cavity and the retina.12-14
In this prospective study, we used commercially available OCT equipment to
improve our understanding of the process of PVD in older persons with healthy
eyes.
SUBJECTS AND METHODS
A prospective study using biomicroscopy and OCT was designed to evaluate
the relationship of the posterior vitreous face relative to the retina in
older persons with healthy eyes. Subjects were recruited on a voluntary basis
and gave informed consent to the study purpose and examinations. A complete
medical and ophthalmic examination included measurement of best-corrected
visual acuity and refraction, slitlamp biomicroscopy with a +90 diopter (D)
lens, and indirect ophthalmoscopy. Individuals were excluded if they had corrected
visual acuity of less than 20/20, intraocular pressure of 22 mm Hg or higher,
a remarkable eye disorder such as cataract or retinal detachment, or systemic
diseases such as diabetes mellitus or systemic hypertension. Therefore, 209
subjects (165 men and 44 women) were enrolled in the study. The mean age was
52.3 years (range, 31-74 years). Only the right eye of each subject was examined
by OCT. The mean refractive error was –1.42 D (range, +5.0 D to –10.75
D). One hundred ninety-three eyes (92.3%) had refractive errors between +3.0
D and –3.0 D; 16 eyes (7.7%) with larger refractive errors were included
in the study because they had corrected visual acuity of 20/20 or better.
Optical coherence tomography was performed in all eyes by a single operator
(E.U.), using commercially available equipment (Humphrey Instruments, Division
of Carl Zeiss; San Leandro, Calif) to obtain axial views of the vitreoretinal
interface in the posterior fundus. After pupillary dilation with a mixture
of 0.5% phenylephrine hydrochloride and 0.5% tropicamide (Mydrin-P; Santen
Pharmaceuticals, Osaka, Japan), we obtained a series of at least 6 images
of 7 mm in length through the center of the fovea along the horizontal and
vertical axes, each overlapped to evaluate the widest possible area of the
posterior fundus, as illustrated in Figure
1. To assess the faint reflectivity of the posterior hyaloid, the
incident light was set at its maximum (750 µW), and the focal plane
and polarization of the instrument were adjusted to provide the highest possible
signal. Optical coherence tomographic digital images of the posterior fundus
were processed using commercial software (Adobe Photoshop; Adobe Systems Inc,
San Jose, Calif) to obtain a composite of overlapped images. All images were
assessed independently by 2 of us (E.U. and A.U.) relative to the vitreoretinal
interface and, in particular, the discrete linear signals in the posterior
vitreous cavity, believed to represent the posterior hyaloid face separated
from the retina.14-15 In addition,
the extent of PVD was evaluated by measuring the distance between the detached
posterior vitreous face and the retina. Data were analyzed using  2 test and analysis of variance.
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Figure 1. The area of optical coherence
tomographic scanning. A series of images 7 mm in length was obtained in each
subject through the fovea along the horizontal and vertical axes; each overlapped
to evaluate the widest possible area of the posterior fundus.
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RESULTS
Optical coherence tomography of the posterior vitreous cortex in 209
healthy eyes of 209 adults with healthy eyes showed either optically empty
space or a discrete linear signal (Figure
2). The discrete linear signal was blue or blue-green, sharply defined,
and localized up to about 800 µm from the retinal surface, forming a
convexoconvex or planoconvex clear space by attachment to the posterior and
midperipheral retina. The discrete linear signal was reproducible. Based on
the location and extent of the signal, the condition of the posterior vitreous
was classified as 1 of 5 stages: no PVD (stage 0), incomplete PVD (stages
1, 2, and 3), or complete PVD (stage 4).
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Figure 2. Optical coherence tomographic
images illustrating various stages of posterior vitreous detachment (PVD).
A, Stage 0, no PVD. B, Stage 1, incomplete PVD in the temporal perifovea,
with a definite discrete linear signal (68 µm from the retinal surface),
with attachment to the fovea, optic nerve head, and midperipheral retina.
C, Stage 2, incomplete PVD in the temporal and nasal perifovea, with convex
retrovitreous spaces associated with attachment of the posterior vitreous
face to the fovea and midperipheral retina. D, Stage 3, incomplete PVD over
the posterior pole, with persistent attachment to the optic nerve head.
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Stage 0 was defined by the absence of PVD (Figure 2A). At this stage, there was no discrete linear signal on
any images along the horizontal or vertical axis. Some eyes at this stage
had random signals over the retinal surface, presumably representing the posterior
vitreous face firmly attached to the retina.
Stage 1 was defined by focal perifoveal PVD (Figure 2B). This stage showed incomplete PVD that was localized
in the perifovea, with persistent attachment to the fovea, optic nerve head,
and midperipheral retina. Incomplete PVD occurring in 1 to 3 quadrants was
classified as stage 1.
Stage 2 was defined by perifoveal PVD across all quadrants, with persistent
attachment to the fovea, optic nerve head, and midperipheral retina (Figure 2C).
Stage 3 was defined by detachment of the posterior vitreous face from
the fovea, with persistent attachment to the optic nerve head and midperipheral
retina (Figure 2D).
Stage 4 was defined by complete PVD, with biomicroscopically identified
detachment of the posterior vitreous face with Weiss ring. However, OCT at
this stage failed to detect any discrete linear signal because the distance
from the retina was outside of the range of OCT.
Of the 209 eyes, 61 (29.2%) were stage 0; 100 (47.8%), stage 1; 26 (12.4%),
stage 2; 4 (1.9%), stage 3; and 18 (8.6%), stage 4, with complete PVD. One
hundred thirty eyes (62.2%) with incomplete PVD (stages 1-3) were asymptomatic,
and none had any biomicroscopic evidence of PVD or Weiss ring. All eyes with
complete PVD showed Weiss ring on biomicroscopy.
Figure 3 illustrates the incidence
of incomplete or complete PVD relative to the subjects' age decade. Stage
1 PVD was found in half of subjects in their fourth decade. With age, the
number of subjects with no PVD decreased, while the number with incomplete
or complete PVD increased. Although the number of subjects older than 60 years
was small, an age-related progression from no PVD through incomplete PVD to
complete PVD was significant.
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Figure 3. Incidence of stages of the vitreoretinal
interface relative to the subjects' age by decade, as seen by optical coherence
tomography. Stage 0, no posterior vitreous detachment (PVD); stages 1, 2,
and 3, incomplete PVD; and stage 4, complete PVD. A 2 test
of data grouped by stage (stages 0, 1-3, and 4) and age (30-49, 50-59, and
60-79 years) shows a significant age-related increase in the number of advanced
stages (24 = 12.31, P = .02).
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The site and extent of incomplete PVD were variable among eyes. Of 100
stage 1 eyes, 46 had incomplete PVD in 1 quadrant, 26 in 2 quadrants, and
28 in 3 quadrants. Twenty-six stage 2 eyes had, by definition, incomplete
PVD in all quadrants. The extent of PVD in these eyes was determined with
OCT by measuring the maximum distance (in micrometers) between the discrete
linear signals and the retina (Figure 2).
Among stage 1 eyes, the mean (SD) distance was 97.6 (47.9) µm in 46
eyes involving 1 quadrant, 115.0 (69.4) µm in 26 eyes involving 2 quadrants,
122 (89.6) µm in 28 eyes involving 3 quadrants, and among 26 stage 2
eyes, the mean distance was 143.8 (100.4) µm. A statistically significant
increase in magnitude was noted between the stages of incomplete PVD (1-way
analysis of variance, P = .02). The magnitude of
incomplete PVD increased significantly from stage 1 involving 1 quadrant to
stage 2 (P = .002), and from stage 1 involving 2
quadrants to stage 2 (P = .048).
To determine whether there is any geographic predilection for the initial
development of PVD, a series of OCT images through the fovea along the horizontal
and vertical axes was evaluated for the quadrant affected with stage-1 incomplete
PVD. The results are shown in Figure 4.
There was a statistically significant predilection for the superior quadrant.
Furthermore, the extent of incomplete PVD was significantly greater in the
superior quadrant, as shown in Figure 5.
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Figure 4. Geographical distribution of stage
1 incomplete posterior vitreous detachment (PVD). The incidence is shown in
3 groups: 46 regions of 46 eyes involving 1 quadrant, 52 regions of 26 eyes
involving 2 quadrants, and 84 regions in 28 eyes involving 3 quadrants. Involvement
of the superior quadrant is significantly frequent in all groups (2 test, P<.001 for all groups).
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Figure 5. Quadrants of incomplete posterior
vitreous detachment (PVD) and distance in micrometers between the discrete
linear signal and retina. Data were collected from 100 eyes with incomplete
PVD: superior quadrant, mean (SD), 152.1 (99.9) µm, measured in 167
sites in 87 eyes; inferior quadrant, 107.9 (68.6) µm, in 87 sites in
32 eyes; temporal quadrant, 113.6 (74.6) µm, in 86 sites in 34 eyes;
and nasal quadrant, 98 (73.0) µm, in 67 sites in 29 eyes. The magnitude
of incomplete PVD was significantly greater in the superior quadrant (1-way
analysis of variance, P<.001).
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COMMENT
These results elucidate the anatomical properties and evolution of PVD
in adults with healthy eyes. A reproducibly observed, remarkable finding was
a discrete linear signal in the posterior vitreous cavity, characterized by
a blue or blue-green weak intensity in the false-color display system of the
OCT instrument and distinguished from random noise signals in the vitreous
cavity. Similar characteristic vitreous signals on OCT have been described
previously, termed posterior hyaloid membrane or discrete linear signals, and are believed to represent
a detached posterior vitreous face.13-15
The condition of the vitreoretinal interface is staged according to
OCT findings. In this study, many healthy eyes without biomicroscopic identification
of PVD had shallow vitreous detachment in the macular area in varying degrees.
In addition, PVD begins at younger ages than previously thought, with more
than half of individuals younger than 50 years showing asymptomatic, initial
PVD localized in the perifovea, with a significant age-dependent, slow progression
to advanced stages in subsequent decades. Subclinical or occult PVD, as observed
by OCT, has also been reported in the healthy fellow eyes of patients with
macular holes.14-15 Gaudric et
al14 detected initial stages of vitreous separation
in 45 of 61 eyes: 26 with perifoveal hyaloid detachment, corresponding to
stage 1 or stage 2 in this study, and 19 with central hyaloid detachment,
corresponding to stage 3. The present study is the first, to our knowledge,
to evaluate the initial occurrence and progressive development of PVD in a
large number of older persons with healthy eyes, as seen by OCT.
Previous studies3-8
have reported age-dependent PVD in older populations with or without vitreoretinal
disease, describing a prevalence of 50% or more in individuals aged 70 years
and older. Posterior vitreous detachment is usually subdivided into partial
and complete forms.16-17 However,
most data concern complete PVD, with little information available about the
prevalence of the earlier phase of PVD in eyes without vitreoretinal disease,
presumably because of the difficulties in obtaining biomicroscopic evidence
of partial or incomplete PVD. Recently, Kakehashi et al17
examined a large cohort of eyes with and without vitreoretinal disease using
biomicroscopy and photography and reported that partial PVD without thickened
vitreous cortex was found in 44% of eyes without any ocular disease. They
speculated that this type of PVD might be a transition phase to complete PVD.
In our study, obvious partial PVD without thickened vitreous cortex was not
detected on biomicroscopy. A reason for the discrepancy may be that the mean
age of the subjects in the present study was younger than that of the patients
described in the report by Kakehashi et al (52.3 years vs 62.5 years). Incomplete
or subclinical PVD, as seen on OCT, is considered a form of partial PVD without
thickened vitreous cortex. Stage 3 incomplete PVD may be visible on biomicroscopy
when extensive, but we found no biomicroscopic abnormalities in those eyes.
The pathophysiologic mechanism of the development of PVD is beyond the
scope of this study. However, some aspects warrant discussion. Aging of the
vitreous and vitreoretinal interface, with liquefaction of the vitreous and
weakened adhesion of the internal limiting membrane, is thought to be responsible
for the development of PVD.11, 18
We believe that subclinical PVD is also caused by other age-dependent changes
of the vitreous, such as vitreous shrinkage and weakening of vitreoretinal
adhesion, which may pull the posterior vitreous forward and result in its
slight detachment. Morphologic changes of the vitreous body, as visualized
by OCT, may begin in most individuals before age 50.
Age-related PVD is believed to occur as an acute event. Lindner4 and Eisner9 described
such precipitating events as a tear formed in the posterior cortical vitreous
in the region of the macula, through which liquefied vitreous passes to the
vitreous cortex, followed by separation of the surrounding cortical vitreous
from the retina. Eisner referred to this as rhegmatogenous
PVD. Acute PVD usually results in extensive separation of the vitreous
gel from the retina posterior to the vitreous base, in particular the superior
quadrants. However, our results indicate that age-related PVD is not acute
but insidious, so that it occurs initially in the perifovea as a focal, shallow
PVD, extends slowly as subclinical PVD for years without any visual symptoms,
and eventually results in complete PVD on acute release of the vitreopapillary
adhesion of the posterior vitreous face.
The OCT images in this study provide new information about the evolutionary
process of PVD in healthy eyes. It has been suggested that age-related PVD
begins in the posterior pole.1-2,19-20
Optical coherence tomography images by Gaudric et al14
of healthy fellow eyes of patients with idiopathic macular hole showed partial
posterior hyaloid detachment beginning around the macula, usually on its nasal
side. The present results demonstrate that the initial occurrence of occult
PVD is predominantly in the perifovea of the superior quadrant. In addition,
the extent is initially small and becomes larger with progressive extension
of the PVD.
Based on the present findings, a schema of the age-related evolution
of PVD in otherwise healthy eyes is presented in Figure 6. The initial site of PVD is the perifovea, seen as a shallow,
convexoconvex or planoconvex retrohyaloid space in a single quadrant, predominantly
its upper site, followed by a gradual progression over many years to involve
all quadrants, with persistent attachment to the fovea and to the margin of
the optic disc. Throughout these stages, the separation of the posterior vitreous
face remains focal in the posterior pole of the fundus, corresponding to partial
PVD in the classification system, although midperipheral and peripheral conditions
are not informative with OCT because of instrument limitations. Eventually,
the evolution of PVD results in separation from the optic disc margin and
leads to clinically identifiable PVD, with acute signs and symptoms.
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Figure 6. A schematic portrayal of the development
of age-related posterior vitreous detachment (PVD), as seen by optical coherence
tomography. A, Vitreoretinal interface without PVD. B, Posterior vitreous
detachment initially occurs in the perifovea, with a predilection for the
superior quadrant. C, Detachment extends widely in the perifovea, with persistent
attachment to the fovea and optic nerve head. D, Detachment occurs in the
fovea, with persistent attachment of the posterior vitreous face to the optic
nerve head. E, Detachment is completed in association with release of the
vitreopapillary adhesion.
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This study assessed the evolution of PVD in healthy adults. Separation
of the posterior vitreous face plays a role in the underlying cause of age-related
vitreoretinal disorders, such as idiopathic macular hole and vitreomacular
traction syndrome.15 None of our subjects with
OCT-observed separation of the posterior vitreous face showed any disruptive
change in the high-resolution cross-sectional images of the retina. Optical
coherence tomographic images of healthy-appearing fellow eyes of patients
with idiopathic macular hole sometimes demonstrate minimal macular change,
associated with incomplete PVD.14-15
High-resolution evaluation of the vitreoretinal interface using OCT may provide
useful information about the pathogenesis of various vitreoretinal disorders.
AUTHOR INFORMATION
Accepted for publication May 10, 2001.
Corresponding author and reprints: Norio Ohba, MD, PhD, Department
of Ophthalmology, Kagoshima University Faculty of Medicine, 8-35-1 Sakuragaoka,
Kagoshima-shi, Kagoshima 890-8520, Japan (e-mail: ohba{at}med5.kufm.kagoshima-u.ac.jp).
From the Department of Ophthalmology, Kagoshima University Faculty
of Medicine, Kagoshima, Japan.
REFERENCES
| |
1. Foos RY. Posterior vitreous detachment. Trans Am Acad Ophthalmol Otolaryngol. 1972;76:480-497.
PUBMED
2. Foos RY, Wheeler NC. Vitreoretinal juncture: synchysis senilis and posterior vitreous detachment. Ophthalmology. 1982;89:1502-1512.
ISI
| PUBMED
3. Pischel DK. Detachment of the vitreous as seen with slit-lamp examination. Trans Am Ophthalmol Soc. 1952;50:329-346.
PUBMED
4. Lindner B. Acute posterior vitreous detachment and its retinal complications. Acta Ophthalmol. 1966;87(suppl):1-108.
5. O'Malley P. The pattern of vitreous syneresis: a study of 800 autopsy eyes. In: Irvine AR, O'Malley C, eds. Advances in Vitreous
Surgery. Springfield, Ill: Charles C Thomas; 1976:17-33.
6. Weber-Krause B, Eckardt C. Incidence of posterior vitreous detachment in the elderly. Ophthalmologe. 1997;94:619-623.
PUBMED
7. Hikichi T, Hirokawa H, Kado M, et al. Comparison of the prevalence of posterior vitreous detachment in whites
and Japanese. Ophthalmic Surg. 1995;26:39-43.
PUBMED
8. Yonemoto J, Ideta H, Sasaki K, Tanaka S, Hirose A, Oka C. The age of onset of posterior vitreous detachment. Graefes Arch Clin Exp Ophthalmol. 1994;232:67-70.
PUBMED
9. Eisner G. Biomicroscopy of the Peripheral Fundus. New York, NY: Springer-Verlag; 1973.
10. Eisner G. Posterior vitreous detachment. Klin Monatsbl Augenheilkd. 1989;194:389-392.
PUBMED
11. Sebag J. Classifying posterior vitreous detachment: a new way to look at the
invisible. Br J Ophthalmol. 1997;81:521-522.
FREE FULL TEXT
12. Hee MR, Puliafito CA, Wong C, et al. Optical coherence tomography of macular holes. Ophthalmology. 1995;102:748-756.
ISI
| PUBMED
13. Puliafito CA, Hee MR, Schuman JS, et al. Optical Coherence Tomography of Ocular Diseases. SLACK Inc: Thorofare, NJ; 1996.
14. Gaudric A, Haouchine B, Massin P, Paques M, Blain P, Erginay A. Macular hole formation: new data provided by optical coherence tomography. Arch Ophthalmol. 1999;117:744-751.
FREE FULL TEXT
15. Chauhan DS, Antcliff RJ, Rai PA, Williamson TH, Marshall J. Papillofoveal traction in macular hole formation: the role of optical
coherence tomography. Arch Ophthalmol. 2000;118:32-38.
FREE FULL TEXT
16. Tolentino FI, Schepens CL, Freeman HM. Vitreoretinal Disorders: Diagnosis and Management. Philadelphia, Pa: WB Saunders; 1976:130-150.
17. Kakehashi A, Kado M, Akiba J, Hirokawa H. Variations of posterior vitreous detachment. Br J Ophthalmol. 1997;81:527-532.
FREE FULL TEXT
18. Sebag J. The Vitreous: Structure, Function, and Pathobiology. New York, NY: Springer-Verlag; 1989.
19. Foos RY. Posterior vitreous detachment. Trans Am Acad Ophthalmol Otolaryngol. 1972;76:480-497.
20. Avila MP, Jalkh AE, Murakami K, Trempe CL, Schepens CL. Biomicroscopic study of the vitreous in macular breaks. Ophthalmology. 1983;90:1277-1283.
ISI
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